Krill Oil, Fish Oil or BOTH ?
Unlike fish oil supplements made from fatty fish like salmon and sardines, krill oil is made from tiny shrimp-like crustaceans. Both provide EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid), the two omega-3 fatty acids found in fish. The concentration of omega-3 fatty acids, namely EPA and DHA are much lower in krill oil than fish oil.
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Enhanced increase of omega-3 index in healthy individuals with response to 4-week n-3 fatty acid supplementation from krill oil versus fish oil.
BACKGROUND:
Due to structural differences, bioavailability of krill oil, a phospholipid based oil, could be higher than fish oil, a triglyceride-based oil, conferring properties that render it more effective than fish oil in increasing omega-3 index and thereby, reducing cardiovascular disease (CVD) risk.
OBJECTIVE:
The objective was to assess the effects of krill oil compared with fish oil or a placebo control on plasma and red blood cell (RBC) fatty acid profile in healthy volunteers.
PARTICIPANTS AND METHODS:
Twenty four healthy volunteers were recruited for a double blinded, randomized, placebo-controlled, crossover trial. The study consisted of three treatment phases including krill or fish oil each providing 600 mg of n-3 polyunsaturated fatty acids (PUFA) or placebo control, corn oil in capsule form. Each treatment lasted 4 wk and was separated by 8 wk washout phases.
RESULTS:
Krill oil consumption increased plasma (p = 0.0043) and RBC (p = 0.0011) n-3 PUFA concentrations, including EPA and DHA, and reduced n-6:n-3 PUFA ratios (plasma: p = 0.0043, RBC: p = 0.0143) compared with fish oilconsumption. Sum of EPA and DHA concentrations in RBC, the omega-3 index, was increased following krill oilsupplementation compared with fish oil (p = 0.0143) and control (p < 0.0001). Serum triglycerides and HDL cholesterol concentrations did not change with any of the treatments. However, total and LDL cholesterol concentrations were increased following krill (TC: p = 0.0067, LDL: p = 0.0143) and fish oil supplementation (TC: p = 0.0028, LDL: p = 0.0143) compared with control.
CONCLUSIONS:
Consumption of krill oil was well tolerated with no adverse events. Results indicate that krill oil could be more effective than fish oil in increasing n-3 PUFA, reducing n-6:n-3 PUFA ratio, and improving the omega-3 index.
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Neuroprotective effect of astaxanthin (found in krill oil) against rat retinal ganglion cell death under various stresses that induce apoptosis and necrosis.
Abstract
PURPOSE:
Astaxanthin is a type of carotenoid known to have strong antioxidant effects. The purpose of this study was to investigate whether astaxanthin confers a neuroprotective effect against glutamate stress, oxidative stress, and hypoxia-induced apoptotic or necrotic cell death in primary cultures of rat retinal ganglion cells (RGCs).
RESULTS:
We found that under glutamate stress, RGC viability was reduced to 58%. Cultures with 1 nM, 10 nM, and 100 nM astaxanthin showed an increase in RGC viability of 63%, 74%, and 84%, respectively. Under oxidative stress, RGC viability was reduced to 40%, and astaxanthin administration resulted in increased viability of 43%, 50%, and 67%, respectively. Under hypoxia, RGC viability was reduced to 66%, and astaxanthin administration resulted in a significant increase in viability to 67%, 77%, and 93%, respectively. These results indicate that 100 nM astaxanthin leads to a statistically significant increase in RGC viability under the three kinds of stressors tested, compared to controls (Dunnett’s test, p<0.05). The apoptotic activity of RGCs under glutamate stress increased to 32%, but was reduced to 15% with 100 nM astaxanthin administration. Glutamate stress led to a 58% increase in DNA damage, which was reduced to 43% when cultured with 100 nM astaxanthin. Thus, 100 nM astaxanthin showed a statistically significant reduction in apoptosis and DNA damage in RGCs (Wilcoxon rank-sum test, p<0.05).
CONCLUSIONS:
Our results suggest that astaxanthin has a neuroprotective effect against RGC death induced by glutamate stress, oxidative stress, and hypoxia, which induce apoptotic and necrotic cell death.
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